{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T06:46:26Z","timestamp":1779345986461,"version":"3.51.4"},"reference-count":36,"publisher":"Rockefeller University Press","issue":"9","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,5,2]]},"abstract":"<jats:p>Effective priming of T cell responses depends on cognate interactions between naive T cells and professional antigen-presenting cells (APCs). This contact is the result of highly coordinated migration processes, in which the chemokine receptor CCR7 and its ligands, CCL19 and CCL21, play a central role. We used the murine Listeria monocytogenes infection model to characterize the role of the CCR7\/CCR7 ligand system in the generation of T cell responses during bacterial infection. We demonstrate that efficient priming of naive major histocompatibility complex (MHC) class Ia\u2013restricted CD8+ T cells requires CCR7. In contrast, MHC class Ib\u2013restricted CD8+ T cells and MHC class II\u2013restricted CD4+ T cells seem to be less dependent on CCR7; memory T cell responses are independent of CCR7. Infection experiments with bone marrow chimeras or mice reconstituted with purified T cell populations indicate that CCR7 has to be expressed on CD8+ T cells and professional APCs to promote efficient MHC class Ia\u2013restricted T cell priming. Thus, different T cell subtypes and maturation stages have discrete requirements for CCR7.<\/jats:p>","DOI":"10.1084\/jem.20041204","type":"journal-article","created":{"date-parts":[[2005,4,26]],"date-time":"2005-04-26T00:24:36Z","timestamp":1114475076000},"page":"1447-1457","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":52,"title":["Differential requirements for the chemokine receptor CCR7 in T cell activation during <i>Listeria monocytogenes<\/i> infection"],"prefix":"10.1084","volume":"201","author":[{"given":"Mischo","family":"Kursar","sequence":"first","affiliation":[{"name":"1Department of Immunology, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Uta E.","family":"Ho\u0308pken","sequence":"additional","affiliation":[{"name":"2Department for Molecular Tumor Genetics and Immunogenetics, Max-Delbru\u0308ck Center for Molecular Medicine, 13092 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Markus","family":"Koch","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne","family":"Ko\u0308hler","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"Lipp","sequence":"additional","affiliation":[{"name":"2Department for Molecular Tumor Genetics and Immunogenetics, Max-Delbru\u0308ck Center for Molecular Medicine, 13092 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan H.E.","family":"Kaufmann","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans-Willi","family":"Mittru\u0308cker","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[2005,4,25]]},"reference":[{"key":"2023072513022071200_BIB1","doi-asserted-by":"crossref","first-page":"117","DOI":"10.1034\/j.1600-065X.2003.00073.x","volume":"195","year":"2003","journal-title":"Immunol. 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